Percutaneous transluminal coronary angioplasty (PTCA) has become an attractive alternative for treating coronary artery disease (CAD) in older individuals because it is associated with less morbidity and mortality than bypass surgery. However, restenosis following PTCA, occurring in 30-50% of all patients, is the major factor limiting long term success of this procedure. Although advanced age is a major risk factor for atherosclerosis, it is not known if the elderly are at more risk for restenosis than younger populations. Therefore, elucidating the effect of advanced age on restenosis will provide important information in advising older individuals on the long term sequelae of PTCA. Aging is known th result in changes in the vessel wall which might alternatively effect the response to vascular injury. Such changes include an increase in vessel wall diameter, thickness and stiffness. In addition to these changes, aging also increases the expression of growth factors such as TGF-BETA1 the PDGF receptor BB. Therefore, we hypothesized that these changes would alter the response to vascular remodelling following injury and possibly impart an additional risk to restenosis. In order to investigate the effect of age on restenosis, we chose the rat carotid artery model of restenosis. In contrast to previous studies using injury to the rat aorta as a model of restenosis, our results revealed that at early time points following injury, vascular smooth muscle cell (VSMC) migration and intimal thickening was greater in young animals without significant differences in medial VSMC proliferation. However at later time points, no age-associated differences were observed. Mechanisms underlying the initial delay in VSMC migration in old animals are not completely understood, but may be partly due to differences in extracellular matrix (ECM) composition, interactions of the ECM with VSMCs in the vessel wall, and the elaboration of proteases required for VSMC migration. These studies highlight important age-associated differences in the response to vascular injury which will be exploited to further characterize the cellular and molecular mechanisms that underlie restenosis.